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Obesity is increasing worldwide. The addition of excess calorie intake and unhealthy human behavior leads to also other diseases such as metabolic syndromes and liver disease such as non-alcoholic fatty liver disease. Furthermore, the accumulation of fat triggers specific mechanisms that, if prolonged, can cause tissue damage. For instance, the innate immune system becomes agitated in patients with NAFLD or obesity due to excessive fat accumulation. This leads to inflammation in specific tissues and infiltration of other immune cells. One of the main immune cells are neutrophils, which secrete a protease enzyme called protease neutrophil elastase. Interestingly, there have been studies conducted that have shown that when neutrophil elastase is knocked out in mouse models that mimic NAFLD, there seems to be a protective effect occurring in the body and lessen tissue scarring. A possible explanation, and the aim of this thesis, is to explore if autophagy is regulated and thus plays a role in protecting liver from inflammation and fibrosis. Western blotting approach was used to test this hypothesis. The protein samples that are used are extracted from neutrophil elastase knockout mice that have been fed a high-fat high-fructose diet and compare them to samples from wild-type control mice that have been fed a normal chow diet, high-fat diet, and high fat high fructose diet. The results indicated that potential upregulation of the autophagy pathway in the liver of neutrophil elastase knockout mice and more studies would need before accurately and reliably acknowledging the alternation of the autophagy pathway in the liver from mouse model of NAFLD and when neutrophil elastase is knocked out. / 2023-12-10T00:00:00Z

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